What is new about diet in hepatic encephalopathy

Merli, Manuela; Iebba, Valerio; Giusto, M.

doi:10.1007/s11011-015-9734-5

Cited by 32 publications

(20 citation statements)

References 48 publications

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“…It is possible that the combination of skeletal muscle loss and increased fat mass may contribute to the development of metabolic components including insulin resistance, diabetes mellitus, hyperlipidemia and possibly NAFLD but whether there is a common underlying mechanism for both sarcopenia and obesity is still not known[108]. …”

Section: Mechanisms Of Skeletal Muscle Loss In Cirrhosismentioning

confidence: 99%

Sarcopenia from mechanism to diagnosis and treatment in liver disease

Dasarathy

Merli

2016

Journal of Hepatology

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492

578

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Sarcopenia or loss of skeletal muscle mass is the major component of malnutrition and is a frequent complication in cirrhosis that adversely affects clinical outcomes including survival, quality of life, development of other complications and post liver transplantation survival. Radiological image analysis is currently used to diagnose sarcopenia in cirrhosis. Nutrient supplementation and physical activity are used to counter sarcopenia but have not been consistently effective because the underlying molecular and metabolic abnormalities persist or are not influenced by these treatments. Even though alterations in food intake, hypermetabolism, alterations in amino acid profiles, endotoxemia, accelerated starvation and decreased mobility may all contribute to sarcopenia in cirrhosis, hyperammonemia as a possible mediator of the liver-muscle axis has recently gained attention Increased muscle ammonia causes: cataplerosis of α-ketoglutarate, increased transport of leucine in exchange for glutamine, impaired signaling by leucine, increased expression of myostatin, a TGFβ superfamily member and an increased phosphorylation of eukaryotic initiation factor 2α, mitochondrial dysfunction, increased reactive oxygen species that decrease protein synthesis and increased autophagy mediated proteolysis. These molecular and metabolic alterations may contribute to the anabolic resistance and inadequate response to nutrient supplementation in cirrhosis. Central and skeletal muscle fatigue contributes to impaired exercise capacity and responses. Use of proteins with low ammoniagenic potential, leucine enriched amino acid supplementation, long term ammonia lowering strategies and a combination of resistance and endurance exercise to increase muscle mass and function may target the molecular abnormalities in the muscle. Strategies targeting endotoxemia and the gut microbiome need further evaluation.

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Section: Mechanisms Of Skeletal Muscle Loss In Cirrhosismentioning

confidence: 99%

Sarcopenia from mechanism to diagnosis and treatment in liver disease

Dasarathy

Merli

2016

Journal of Hepatology

Self Cite

492

578

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Section: Altered Intestinal Functionmentioning

confidence: 99%

Nutrition and Muscle in Cirrhosis

Anand

2017

Journal of Clinical and Experimental Hepatology

133

154

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As the cirrhosis progresses, development of complication like ascites, hepatic encephalopathy, variceal bleeding, kidney dysfunction, and hepatocellular carcinoma signify increasing risk of short term mortality. Malnutrition and muscle wasting (sarcopenia) is yet other complications that negatively impact survival, quality of life, and response to stressors, such as infection and surgery in patients with cirrhosis. Conventionally, these are not routinely looked for, because nutritional assessment can be a difficult especially if there is associated fluid retention and/or obesity. Patients with cirrhosis may have a combination of loss of skeletal muscle and gain of adipose tissue, culminating in the condition of "sarcopenic obesity." Sarcopenia in cirrhotic patients has been associated with increased mortality, sepsis complications, hyperammonemia, overt hepatic encephalopathy, and increased length of stay after liver transplantation. Assessment of muscles with cross-sectional imaging studies has become an attractive index of nutritional status evaluation in cirrhosis, as sarcopenia, the major component of malnutrition, is primarily responsible for the adverse clinical consequences seen in patients with liver disease. Cirrhosis is a state of accelerated starvation, with increased gluconeogenesis that requires amino acid diversion from other metabolic functions. Protein homeostasis is disturbed in cirrhosis due to several factors such as hyperammonemia, hormonal, and cytokine abnormalities, physical inactivity and direct effects of ethanol and its metabolites. New approaches to manage sarcopenia are being evolved. Branched chain amino acid supplementation, Myostatin inhibitors, and mitochondrial protective agents are currently in various stages of evaluation in preclinical studies to prevent and reverse sarcopenia, in cirrhosis.

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“…From this viewpoint, an improvement in nutritional status and muscle mass can be considered a potential goal to ameliorate the cognitive function in cirrhotic patients and a modulation of diet may represent a promising option when seeking to prevent HE. 52 At the same time, a reduction in ammonia levels may ameliorate muscle wasting. 53…”

Section: Ammonia Metabolism and Traffickingmentioning

confidence: 99%

“…Additional benefits of a vegetal-enriched diet may derive from the modulation of gut microbiota. 52 In decompensated cirrhosis alterations in gut microbiota are frequent, and modulation of gut microbiota may be effective for treating and preventing HE. 58 Prebiotics and probiotics have also been proposed to be useful in preventing HE and MHE, but more studies are required.…”

Section: Nutritional Measuresmentioning

confidence: 99%